Protein Power: The High-Protein Low-Carbohydrate Way to Lose Weight, Feel Fit, and Boost Your Health--in Just Weeks!

Protein Power Succeeds where low-fat diets fail you complete, satisfying meal plans, suitable for family dinners or formal entertaining a Daily Meal Outline to keep track of your food selections ways to modify the foods you love the most to make them fit your diet plan tips on making the best selections at fine restaurants or fast-food chains a minicookbook lled with nearly 100 easy-to-prepare, inexpensive, and mouthwatering recipes, from Tex-Mex Cheese Flan with Chunky Salsa and Coconut Salmon to Irish Lace Cookies and Chocolate Chip Cheesecake supplements that will jump-start your metabolism to burn fat ways to include wine in your diet for enjoyment and health an invaluable program of strength-building exercises tips for maintaining motivation and more

BY THE SAME AUTHORS

M ICHAEL R. EADES, M.D. Thin So Fast M ARY DAN EADES, M.D. If It Runs in Your Family: Breast Cancer If It Runs in Your Family: Arthritis Freeing Someone You Love from Eating Disorders The Doctor’s Complete Guide to Vitamins and Minerals

To British physician John Yudkin, M.D., Ph.D., who was ghting the good ght before we were born. And to our sons, Ted, Daniel, and Scott Eades, who will continue to fight it after we’re gone.

There was an old man of Tobago, Who lived on rice, gruel, and sago; Till, much to his bliss, His physician said this— To a leg, sir, of mutton you may go. JOHN M ARSHALL, 1822

Contents Acknowledgments Introduction PART I: ASSESSING YOUR RISK Chapter 1 A New Nutritional Perspective Chapter 2 The Symptom Treatment Trap Chapter 3 Excess Insulin and the Insulin Resistance Syndrome Chapter 4 Assessing Your Risk PART II: THE PROTEIN POWER PLAN Chapter 5 Putting It All Together: Designing Your Food Plan Chapter 6 Vitamins, Minerals, and Potassium Chapter 7 The Antiaging Formula: Exercise Chapter 8 Motivation: Plan Your Work and Work Your Plan Chapter 9 Sample Menus Chapter 10 Recipes PART III: WHY THIS PLAN WILL LEAVE YOU HEALTHY AND THIN Chapter 11 The Deadly Diseases of Civilization Chapter 12 The Microhormone Messengers: Meet the Eicosanoids Chapter 13 Cholesterol Madness Epilogue: Overcoming the Curse of the Mummies Appendix: Sources and Resources

Acknowledgments We would like to thank the many people who were instrumental in helping us bring this book to you. It’s been a long and sometimes di cult process through which we had the unfailing support of our agent and friend Channa Taub, who consoled and cajoled us through some stressful times and was always willing to sharpen her editorial pencil when needed. Channa brought us to Carol Mann, who gets many thanks for bringing our work to the wonderful group at Bantam Books. Thanks to Fran McCullough, our editor, for her interest in and understanding of this project and for all the work she did to streamline and improve the manuscript. And to everyone at Bantam—especially Irwyn Applebaum, Nita Taublib, Allen Goodman, Amanda Mecke, Barb Burg, and Lauren Janis. To our sons, Ted, Dan, and Scott, who put up with erratic family schedules and cranky parents during the writing of this book, we love you. Our faithful sta at the clinic, who elded calls, juggled schedules, and held down the fort while we wrote, deserve special mention— thanks to Rhonda Mallison, Mary Clendaniel, Linda Tullos, Valerie Wilkins, Michelle Denton, and Deya Devorak. Thanks to Barbara Witt, who contributed most of the recipes. We are grateful for the support, help, criticism, and advice from our many professional and scienti c colleagues who read and commented on this manuscript during its writing. Special thanks to Barry Sears, Ph.D., who has helped us re ne our thinking by engaging us in hundreds of hours of how-many-angels-can-dance-on-the-head-of-a-pintype arguments on the merits of our respective dietary philosophies. And to Allen Hill, M.D., whose suggestions and support have been invaluable, we give heartfelt thanks. Not only has he taken much time from his busy practice to read and help improve our manuscript, he has also graciously taken over the care of our patients innumerable times, often at a moment’s notice, during the many absences this project required of us.

And nally, thanks to Cathy Hemming, our erstwhile agent and always our friend, who believed in the merits of this book and this paradigm before anyone else.

Introduction You may be wondering how a couple of physicians who specialize in weight loss in a relatively small city in Middle America devised a nutritional program that works as well as this one does, while most of the scientists in the major universities are headed o in the opposite direction, puzzling over why their success with low-fat diet plans has been so minimal. In a nutshell, we lucked out. We lucked out because that’s how science works. Science progresses because people continue to question why. Researchers propose hypotheses based on their understanding of the natural world and then test them —and most of the time these theories blow up in their faces. The lucky ones stumble onto the hypotheses that turn out to be valid. But of course there’s more than luck involved, because as Louis Pasteur said, “Chance favors the prepared mind,” and in our case our minds were prepared by many years of clinical practice with patients su ering all the illnesses that are heir to disordered insulin metabolism as well as by our unique combination of medical interests. Mike is a collector of diet books and old medical texts and has a strong interest in paleopathology and biochemistry; Mary Dan is interested in anthropology and has published a book on eating disorders and the deranged metabolic status of eating-disordered patients. We have a copy of the earliest diet book ever to sweep the nation, Banting’s Letter on Corpulence, rst printed in the middle 1800s. This restricted-carbohydrate diet worked like a charm for Banting and, if sales were any in duration, many others. It has always intrigued us because it completely ies in the face of today’s low-fat paradigm. At about the same time we ran across Banting we began attending paleopathology conferences and studying anthropology, where we learned what paleopathologists and anthropologists have known for years: the agricultural revolution and the increased consumption of carbohydrates it brought along with it played havoc with the health of early man. Mary Dan’s extensive study of eating disorders and metabolic hormonal derangements combined with

Mike’s interest in biochemistry rounded out the “preparation” of our minds. We looked at Banting’s success with carbohydrate restriction along with the paleopathological/anthropological data showing a decline in health accompanying an increase in carbohydrate intake and concluded that maybe the intake of large amounts of carbohydrates wasn’t necessarily a good thing. That became our rst mini-hypothesis: excess carbohydrate consumption isn’t good. But why not? We knew, as does every doctor, that the immediate e ect of carbohydrate consumption is increased blood glucose, then an increased insulin level. We thought that perhaps the increased insulin levels might be to blame for part of the problem. As we studied the medical literature, we found that researchers the world over were nding elevated insulin levels associated with obesity, heart disease, high blood pressure, and diabetes—the common diseases of modern man. We also found that the same researchers were for the most part trying to treat these patients by giving them more of the same thing we were beginning to believe may have caused the problem in the rst place: the high-carbohydrate, low-fat diet. It made more sense to us that if excess insulin indeed causes these disorders, or at the very least makes them worse, as the increasing mountain of research indicated, perhaps patients would be better o reducing their carbohydrate intake, not increasing it. We took then as our working hypothesis that excess carbohydrate leads to excess insulin, which leads to obesity, high blood pressure, and all the rest. It t with the anthropological and paleopathological data and, at least as far as obesity was concerned, with Banting’s dietary theory. We then began to examine this hypothesis from a basic biochemical perspective and found that it worked beautifully. From all perspectives our hypothesis looked good on paper, so we began to test it carefully, rst on ourselves, then on patients in our practice. We found that the results were rapid, dramatic, and pretty much uniform—just what we expected based on the underlying science. As we worked with our patients, we continued to re ne our techniques, expand our range of dietary choices, and in general

techniques, expand our range of dietary choices, and in general collect those little tips and tricks that make the practice of medicine an art as well as a science. We are still learning and re ning every day, and, as with any technique that works, more and more practitioners are beginning to use a restricted-carbohydrate diet for their patients and are adding their own unique re nements to the rapidly growing body of data. Will this program work for you? In good conscience, we can only say probably. The reason we hedge a little is because of biochemical individuality—we are all as di erent biochemically as we are in appearance. Every doctor has encountered patients in whom medicines seem to work in an opposite fashion to that intended, patients who are kept awake by sleeping pills and pass out on stimulants. These and similar experiences keep practiced physicians from ever making blanket this-will-work-in-all-circum-stances statements. All we can tell you is that in the almost ten years we have been treating patients with this program we have never had a negative outcome. If you’re like the vast majority of our patients, you will nd the results as striking and life changing as we have and will adopt this program, modi ed to your own unique lifestyle and tastes, for the rest of your life. Little Rock June 1995

Part I

Assessing Your Risk

Chapter 1

A New Nutritional Perspective Every man is the creature of the age in which he lives; very few are able to raise themselves above the ideas of the time. VOLTAIRE We have a medical book published in 1822 passed down to Michael from his great-grandfather, a country doctor from the Ozark Mountains. A long section deals with yellow fever—in the 1800s no one knew what caused it or how it spread. Now, of course, we understand that the mosquito is the carrier of the virus that causes yellow fever, but then the cause eluded the best minds in medical science. Read what this standard 1822 medical textbook says about yellow fever: … it rises from the exposure of putrid animal and vegetable substances on the public wharfs … it always begins in the lowest part of a populous mercantile town near the water, and continues here without much a ecting the higher parts. It rages most where large quantities of new ground have been made by banking out the rivers for the purpose of constructing wharfs…. the yellow fever is generated by the impure air or vapour which issues from the new-made earth or ground raised on the muddy and filthy bottom of rivers….

From our contemporary vantage point we want to reach back and tell them, “Look, it’s a mosquito; why can’t you see the big picture?” The medical problems that confound us today will probably amaze scientists in the twenty-first century as they puzzle over why we medical pioneers of today were unable to reach out and grasp the obvious, why we were so advanced in certain areas of medical treatment yet so abysmally de cient in others. Why, they may ask, could our surgeons perform open-heart surgery so skillfully as to make it a routine operation while at the same time our nutritional experts couldn’t determine the optimal diet for preventing most of the problems necessitating that procedure? Why spend so much time and e ort developing complex surgical techniques and other wondrous medical procedures that prolong the life of a diseased body for a few months or, at best, a few years instead of focusing on nutritional changes capable

at best, a few years instead of focusing on nutritional changes capable of prolonging healthy life for decades? Why can’t we see the big picture? The Failure of the Low-Fat High-Carbohydrate Diet Yes, doctors today are aware that diet plays a signi cant role in the development and progression of the major diseases a icting modern man—heart disease, diabetes, obesity, high blood pressure, and many kinds of cancers. As a consequence dietitians, nutritionists, and physicians constantly exhort us to eat properly to avoid these disorders. By their definition, eating properly means rooting out fat from our diets and replacing it with complex carbohydrate. Ever since the surgeon general recommended in 1988 that Americans severely reduce their consumption of fat, especially saturated fat, the race to zero-fat products has been on. Eggs, red meat, and other superior protein sources have been virtually drummed out of the American kitchen. Reduce fat intake to almost nothing, we are told by battalions of nutritional experts, and good-bye obesity, heart disease, diabetes, and all the rest. Sounds great in theory, but—and here’s why physicians a hundred years from now will be shaking their heads—it doesn’t work. The low-fat, high-complex-carbohydrate approach has proven a failure. It doesn’t reduce cholesterol levels to any great degree unless followed to an almost ridiculous extreme, in which case it can actually cause other equally sinister problems, as you will soon discover. It gives diabetes su erers endless grief in trying to regulate their blood sugar levels. It doesn’t reduce high blood pressure unless it brings about signi cant weight loss. Its success rate for weight loss is almost nonexistent. (You may be surprised to learn that we’ve treated many people who have gained weight on the low-fat diet.) The result of the current no-fat mania has been a fatter and less healthy America, thanks in part to the zeal of food manufacturers who have given us an endless variety of fat-free high-carbohydrate junk to replace the fat- lled junk we were eating before.

In the face of this dismal record, what do we as medical professionals do? Do we write off the low-fat diet as something that sounded good on paper but didn’t work in practice, abandon it and begin searching for something better, as we would a new drug that had failed? No. Instead we say, “Bring on more of the same. Let’s try harder, let’s try longer, let’s be more diligent.” We tell our patients that it must be their fault if their condition doesn’t improve on a low-fat diet; they must not be following it correctly. But such thinking ies in the face of metabolic reality because dietary fat alone is not the problem. The problem lies in the biochemical structure of the low-fat diet and the mixed signals it gives to the body’s essential metabolic processes. Ironically, not only does the low-fat diet fail to solve the health problems it addresses; it actually makes them even worse. The program we outline in this book triumphs where the low-fat, high-complex-carbohydrate diet fails. It reduces cholesterol rapidly without increasing other risk factors; it reverses, or at least signi cantly improves, adult-onset (type II) diabetes; it drops elevated blood pressure like a rock; it o ers a long-term solution for the problem of excess weight—all without asking you to count fat grams or worry about fat percentages. It does all this simply by selecting foods that work with your body’s metabolic biochemistry instead of against it. The human body is a remarkably resilient, reactive, regenerative piece of biochemical machinery. Like any piece of complex equipment, it functions best when treated properly. The proponents of low-fat dieting believe the best way to treat the body is by restricting the amount of fat, particularly saturated fat, the body takes in and replacing it with complex carbohydrate. Their awed thinking goes like this: too much fat accumulation in the arteries causes heart disease and other problems, too much fat accumulation in the fat cells causes obesity, and too much fat intake exacerbates diabetes, so if we reduce fat intake, we’ll solve all these problems. Although it seems logical, it doesn’t work because it doesn’t take into account the body’s biochemistry and the ways our metabolic hormones cause us to store fat. When we understand and control these potent body chemicals, we can achieve our health goals by controlling fat from within rather than trying to

our health goals by controlling fat from within rather than trying to eliminate it from without. To begin to understand how this works, let’s first examine food from a biochemical perspective. What Is This Thing Called Food? All food, from pancakes to sushi, is composed of macronutrients, micronutrients, and water. Aside from water, which makes up the lion’s share of everything, food is made primarily of the macronutrients protein, fat, and carbohydrate. These three macronutrients are the only food components that provide energy—measured as calories—to maintain life. The micronutrients—vitamins, minerals, and trace elements—provide no caloric energy but are nevertheless essential for life. They perform a multitude of cellular functions, many of which involve the e cient use and disposal of the macronutrients. Without macronutrients we would su er malnutrition, starvation, and death; without the micronutrients we would su er de ciency diseases, a precipitous health decline, and death. The nutrients from both groups are necessary for life. BALANCING THE BIG THREE Since the entire caloric content of food comes from the three macronutrients, it is obvious that decreasing any one macronutrient— fat, for instance—requires increasing an other (carbohydrate or protein or both) to maintain any given caloric level. If your metabolic needs for a day require 2,000 calories, and, in accordance with the recommendations of the nutritional establishment, you reduce your fat intake, what happens? You increase your intake of carbohydrate and protein to make up for the calories lost by removing the fat, right? Actually, it’s a little more complicated than that. You don’t go to the grocery store and buy three scoops of protein, ve scoops of carbohydrate, and two scoops of fat; you buy meat, eggs, vegetables, fruits, dairy products. Some foods, meat and eggs, for instance, contain only protein and fat, while others such as apples and grapes are

only protein and fat, while others such as apples and grapes are practically all carbohydrate with only a trace of protein. You can trim the visible fat from cuts of meat to reduce fat content, but otherwise it’s di cult to extract just one macronutrient from a particular food item. So the only way to change the ratios of fat, protein, and carbohydrate is to change the types of foods eaten. If you want to decrease your fat intake, you simply eat less meat, eggs, and dairy products and replace them with fruits and vegetables. Sounds reasonable, but is it? Not really, and here’s why. Humans don’t require equal amounts of the three macronutrients for optimal health. The average person requires at least 70 to 100 grams of protein per day, or about 300 calories’ worth, and at least 6 to 10 grams of linoleic acid (a type of fat that is essential to health), about 75 calories’ worth. What about carbohydrate? The actual amount of carbohydrate required by humans for health is zero.1 We haven’t made these figures up; they represent the consensus of scienti c wisdom today. Now, this doesn’t mean that as long as you get 75 grams of protein and 6 grams of fat you’ll do ne. You need more calories to provide energy for your bodily functions. It does mean that if you got enough energy from either protein or fat and maintained your minimum intake of each, you would do ne. Eskimos eat very little carbohydrate, in fact no carbohydrate during the winter, and survive nicely to a ripe old age. Although their traditional diet is composed of a large quantity of protein and an enormous amount of fat, Eskimos suffer very little heart disease, diabetes, obesity (despite the cartoons), high blood pressure, and all the other diseases we associate with a more civilized lifestyle. Furthermore, Eskimos don’t have metabolic systems from an alien planet; they have the exact same biochemistry and physiology that we do. Yes, you could eat the same diet and tolerate it nicely.2 Bearing in mind that protein and fat are essential to health and carbohydrate isn’t, what happens when we cut back our fat as the nutritional establishment recommends? Since we can’t for the most part remove the fat from the food, we end up replacing foods that contain fat with those that don’t. Since most sources of good-quality protein— meat, eggs, and dairy products—contain a fair amount of fat, to cut back on fat we end up cutting back on protein as well and replacing

them both with carbohydrate. Most vegetable sources of protein—beans and grains—are incomplete unless combined carefully and contain far more carbohydrate than protein. In the end if we strictly follow the low-fat prescription we can end up de cient in protein (it’s di cult to be de cient in fat because the only essential fat is linoleic acid, which is found in vegetable oils). But possibly the worst news of all is that eating more carbohydrates stimulates your body’s fat storage. In attempting to reduce fat intake, you wind up actually getting fatter, because some macronutrients stimulate profound metabolic hormonal changes. Surprisingly, fat doesn’t do much. If you were to swill down a dish of lard while hooked up to a laboratory device to measure the levels of your metabolic hormones—chie y insulin and glucagon—you wouldn’t see much activity, because fat is essentially metabolically inert. Carbohydrate, however, would set o a Mad Hatter’s tea party of metabolic activity. Eating a handful of grapes while hooked to the same device would initiate a wild swinging of gauge needles indicating a rapid increase in insulin and a decrease in its opposing hormone glucagon, all perfectly normal metabolic responses kindled by the consumption of carbohydrate. It follows logically that the constant consumption of large quantities of carbohydrate would then produce large quantities of insulin, which indeed it does. Even complex carbohydrates stimulate the response because all carbohydrates are basically sugar. Various sugar molecules—primarily glucose—hooked together chemically compose the entire family of carbohydrates. Your body has digestive enzymes that break these chemical bonds and release the sugar molecules into the blood, where they stimulate insulin and the other metabolic hormones. This means that if you follow a 2,200-calorie diet that is 60 percent carbohydrate— the very one most nutritionists recommend—your body will end up having to contend metabolically with almost 2 cups of pure sugar per day. What’s Insulin Got to Do with It?

So, what does insulin have to do with anything other than diabetes? And if you don’t have diabetes, why should you care about insulin at all? Because it’s important to your health. Insulin, a hormone produced and released into the blood by the pancreas, a ects virtually every cell in the body. Insulin occupies a chapter or two in every medical biochemistry and physiology textbook, entire sections in endocrinology texts, and even two pages of tiny print in our fteen-year-old Encyclopaedia Britannica. Whole textbooks are devoted to its myriad activities. Insulin regulates blood sugar, yes, but it does much more. It controls the storage of fat, it directs the ow of amino acids, fatty acids, and carbohydrate to the tissues, it regulates the liver’s synthesis of cholesterol, it functions as a growth hormone, it is involved in appetite control, it drives the kidneys to retain uid, and much, much more. This master hormone of metabolism is a substance absolutely essential to life; without it, you would perish—quickly. But insulin is also a monster hormone; it has a dark side. In the proper amount it is life sustaining; too much of it causes enormous health problems. Reams of scienti c studies, with more added to the stack daily, implicate excess insulin as a primary cause of or signi cant risk factor for high blood pressure, heart disease, obesity, elevated cholesterol and other blood fats, and diabetes (yes, insulin itself can cause diabetes, a concept we will explore at length later in this book). If you don’t have diabetes now, that doesn’t mean you won’t develop it in the future, especially if it runs in your family. The same goes for heart disease, high blood pressure, and all the rest. Insulin problems have a strong genetic basis, so a good way to determine if you are at risk for any of the insulin-related disorders is to examine your family tree closely. If your parents or grandparents had or have any of the following, you are at risk: heart disease, high blood pressure, accumulation of fat around the waistline, elevated cholesterol,

elevated triglycerides and other blood fats, type II diabetes, excess fluid retention (swelling of ankles). As you consider the health profiles of your family members, be aware that the more of these disorders you identify, the more at risk you are for developing them. If you are at risk, you have a pressing reason to care about insulin, because controlling it can literally save your life; if you have already been a icted with one (or more) of these disorders, controlling your insulin can restore your health. Taming the Monster: Controlling Insulin Through Diet How do you go about controlling it? With our nutritional regimen—a carbohydrate-restricted, moderate-fat, adequate-protein diet that modulates the body’s metabolic hormones, including insulin. Diet is what makes insulin levels go haywire in the rst place, so it stands to reason that dietary changes should be able to reverse the problem. Diet is, in fact, the only way to solve this problem. The foods we eat exert a profound in uence on what happens within our bodies hormonally—both for good and for bad. By eating the correct balance of foods we can almost medicinally alter what goes on inside us in a healthful way; by eating the wrong foods we can precipitate health disasters. We can more easily dig our graves with a fork and spoon than with a shovel. Our plan uses food as a tool to reverse, or at the very least markedly improve, disorders engendered by a metabolic system out of whack. Our easy-to-follow dietary regimen is tasty, lling, nutritionally complete, and even allows for the consumption of alcoholic beverages —in moderation. It works. And best of all it works quickly. How quickly? In terms of feeling better and more energetic, within a week or less; for cholesterol reduction, substantial reductions in blood levels by three weeks, maybe sooner (we say maybe sooner because we’ve never checked anyone before three weeks). Victims of high blood

we’ve never checked anyone before three weeks). Victims of high blood pressure—a condition that is usually insulin related—typically achieve a greatly lowered, or normal, blood pressure within a week or two. Those with diabetes and related problems generally nd their blood sugar levels normalized or at least greatly improved within just a few weeks—sometimes only days. High blood pressure, elevated cholesterol, type II diabetes—this program corrects or greatly improves them all in short order by normalizing the body’s disrupted metabolic hormonal status, which causes all these problems in the first place. Obesity, the other major health problem rooted in a disturbed insulin metabolism, doesn’t disappear as quickly, of course. Although our nutritional program opens all the metabolic pathways to allow an e cient burning of body fat for energy, the body fat still has to be burned—and depending on how much there is to burn, that can take some time. The good news is, however, that long before our patients lose much weight on the program the medical problems a icting most of them—high blood pressure, elevated cholesterol, diabetes, gout, and a host of others—improve dramatically or even vanish. Now, granted, on the typical low-calorie, low-fat, high-complex-carbohydrate weightreduction diet these medical disorders will sometimes gradually improve as body weight falls, but on our diet these improvements are almost immediate due to the rapid metabolic changes effected. Of course we don’t have all the answers; but we do have a nutritional program that we’ve tested on ourselves, our three sons, thousands of our patients, and countless people nationwide, without a single adverse reaction.3 Our approach is scienti cally valid, historically valid, and can be explained using not a few obscure scienti c articles but standard medical textbooks. This is important because it means that we’ve based our conclusions on scienti c fact, not theory. Medical scientists doing cutting-edge research publish their ndings in medical/scienti c journals, initiating a restorm of debate and a urry of activity in other laboratories the world over. Many scientists then repeat the experiments, sometimes obtaining the same results, sometimes not. Before any particular piece of scienti c knowledge is generally considered valid, it must be con rmed by multiple long-term tests,

performed in many di erent labs, all with the same result. Only then does it enter the medical literature as fact, and only then is it published in medical textbooks. Not only can all the concepts underlying our program be found in every basic medical textbook, but studies con rming our approach are beginning to appear throughout the medical journals (again, write to us in care of our publisher for a bibliography). Could anyone have seen this big picture earlier? Interestingly enough, the answer is a quali ed yes. The history of dieting begins in 1825, when the Frenchman Jean-Anthelme BrillatSavarin published an essay entitled “Preventative or Curative Treatment of Obesity” in his gastronomic classic The Physiology of Taste in which he stated: “Now, an antifat diet is based on the commonest and most active cause of obesity, since, as it has already been clearly shown, it is only because of grains and starches that fatty congestion can occur, as much in a man as in the animals; this e ect… plays a large part in the commerce of fattened beasts for our markets, and it can be deduced, as an exact consequence, that a more or less rigid abstinence from everything that is starchy or oury will lead to the lessening of weight.” Brillat-Savarin had obviously empirically stumbled onto the virtues of a restricted-carbohydrate diet and published his ndings. In 1862 William Banting, an upscale London undertaker, found himself so obese that he could not tie his shoes and had to walk downstairs backward. He tried all the fashionable cures of the day without success until his physician put him on a diet free of starchy and sugary foods. Banting followed this diet to the letter and lost a pound a week until he reached a normal weight and restored his health and his ability to walk down the stairs face rst. He was so overjoyed with his success that, at his own expense, he published and distributed 2,500 copies of his Letter on Corpulence, describing his treatment and his own modi cations of the plan. Demand was so great for this pamphlet that it rapidly went through many editions on both sides of the Atlantic before his death in 1878 at eighty-one years of age. His diet was so well known that his name became synonymous with dieting; people weren’t dieting; they were banting. In America, Banting’s lean-meat diet led to the

development of the American Salisbury steak, a staple of life in the late 1800s. The next popular weight loss and health book was Eat and Grow Thin by Vance Thompson, husband of actress Lillian Spencer and founder of M’lle New York magazine. This slim book touting the virtues of a restricted-carbohydrate diet (allegedly written by the Asian sage Mahdah) was an enormous best-seller that went through its 112th printing in 1931. These early diet books all have in common the fact that their authors were untrained as physicians or scientists (Brillat-Savarin was a lawyer) and basically promoted and adhered to these diets simply because they worked, as testi ed to by the hundreds of thousands of “patients” who followed them. In the late 1920s mainstream medical scientists observed and reported on the efficacy of the restricted-carbohydrate diet when the Arctic explorer Vilhjalmur Stefansson and a colleague submitted themselves to a meat-only diet for a year (see footnote 2). In England in more recent times T. L. Cleave, the surgeon-captain of the Royal Navy, and John Yudkin, M.D., Ph.D., professor of nutrition at Queen Elizabeth College, London University, have studied and written extensively on the merits of the restricted-carbohydrate diet. Dr. Yudkin has published papers on restricted-carbohydrate dieting from both a scienti c and a natural history perspective in most of the prestigious medical journals during a career spanning six decades. At eighty-five, he continues to write and publish. His books, This Slimming Business and A-Z of Slimming, are classics on the subject. The three most popular diet books in America in recent years were all written by physicians detailing their own versions of the restrictedcarbohydrate diet. Dr. Irwin Stillman published his Quick Weight Loss Diet in 1967, describing how he overcame middle-aged obesity and a heart attack by cutting carbohydrates and drinking large quantities of water. Dr. Robert Atkins wrote Dr. Atkins’ Diet Revolution, another multimillion-copy best-seller, in 1972, detailing his own experiences as well as those of his many patients with low-carbohydrate dieting. In 1979 Dr. Herman Tarnower explained his approach to lowcarbohydrate dieting with his cardiology and internal medicine patients

carbohydrate dieting with his cardiology and internal medicine patients in The Complete Scarsdale Medical Diet. These books in hardcover and paperback have sold over 20 million copies (amazingly, the last two are still in print twenty years later), and there is probably not a dieter alive who hasn’t at least heard of one of these books, if not all. Why are they so popular? Because they work. None of the authors of any of these popular diet books wrote about the underlying science involved; they just found carbohydrate restriction to be an e ective means to bring about weight loss and health improvement in an easy-to-follow diet. In essence these authors “discovered” by trial and error the same thing that Brillat-Savarin, Banting, and the others found the same way. There has been no doubt that these diets work. The only question has been: why? In the chapters to come, you will learn the biochemistry and physiology of the why. And in learning how carbohydrate restriction works through insulin reduction, you will be able to use our techniques to expand on the restricted programs of those who came before us. First let’s look at the most extensive study of the low-fat, highcomplex-carbohydrate nutritional approach ever undertaken—the civilization of ancient Egypt. You can draw your own conclusions from the pages of history. The Bottom Line At the end of each chapter you’ll nd a succinct summary of everything you need to remember. 1 As you will discover in a later chapter, your body has all the biochemical machinery

necessary to make all the blood sugar you need to nourish the tissues that require it— red blood ceils, some parts of the eye, brain, and kidney. 2 We know this because of the famous study done in 1929 and 1930 using the explorers

Vilhjalmur Stefansson and Karsten Anderson. These men returned from the Arctic reporting that Eskimos were able to live on nothing but caribou meat all winter while performing arduous work, expending great amounts of energy without consequence. To prove that not only Eskimos had this capability, both explorers volunteered to be studied while hospitalized in Bellevue Hospital in New York City for one year. During this time they ate a meat diet composed of more than 2,500 calories a day, which was 75 percent fat. At the end of the year both had lost about 6 pounds of weight, their cholesterol levels and other blood chemistry values were normal, and neither experienced any adverse effects. 3 In 1989 Michael wrote a book, Thin So Fast, published by Warner Books that described our nutritional regimen as applied solely to weight loss. Since then we’ve received countless letters from readers ail over the world, recounting their successes after years of failure on more conventional diets.

Chapter 2

The Symptom Treatment Trap All great truths begin as blasphemies.

GEORGE BERNARD SHAW “You want me to eat what?” The middle-aged lady sitting across the desk from us was incredulous and becoming more so by the second as we explained to her the changes she needed to make in her diet—changes necessary to reduce the dangerously elevated level of fat in her blood. She didn’t have a serious weight problem; she had come to us seeking advice on the treatment of her cholesterol problem, but she was having di culty accepting that advice. “But if I eat all these foods you’re telling me to eat, won’t my cholesterol just go higher? I can’t see how I can eat an egg or red meat in my condition. Are you sure this is going to work?” We explained how her physiology worked and why her cholesterol was high. Her metabolism would change as she followed our nutritional plan, and these changes would result in a dramatic reduction in her cholesterol levels. We told her that once she got started on the proper diet she would see major results within just a few weeks in stead of the months it usually takes for diets to work—if they do at all. Then she could judge for herself whether or not she was on the right track. She may not have been convinced by the scienti c explanations of her problem and its solution, but she brightened at the thought of seeing results so quickly. “Six weeks!? Do you really think I will have improved much by then?” she asked. “You will be pleasantly surprised.” “I hope so. I don’t know if I can go through another experience like the last time. I worked so hard with my previous doctor. I faithfully followed the diet he prescribed, and for what? Practically nothing. I don’t mean to be such a whiner, but you’ve got to understand that I’m at my wit’s end with this. If I don’t get this cholesterol under control

at my wit’s end with this. If I don’t get this cholesterol under control and start feeling better, I’m going to be a basket case.” We certainly understood. Although her problem is more serious than most, Jayne Bledsoe1 is fairly typical of the patients we treat in our metabolic practice. We have heard variations of her history from countless other patients who have gotten stuck on the cholesterol treadmill. Treating the Symptom, Missing the Problem Jayne had been unaware that she even had a problem until she went for a routine physical examination. Her doctor checked her over, told her she appeared to be in good health, drew some blood, and told her he would call her when the results came back from the lab. He called the next day and dropped the bombshell: her blood fats were dangerously elevated. Her serum cholesterol was 750 mg/dl (milligrams/deciliter)—normal is anything below 200 and her triglycerides (another blood fat usually measured in the 100-to-250mg/dl range) were a whopping 3,000 mg/dl! Most physicians get excited over a cholesterol of 300 mg/dl, let alone 750, and become outright alarmed at such a triglyceride level. So it’s no surprise that her doctor—following standard medical protocol—completely bypassed Step One and immediately started her on the National Cholesterol Awareness Program Step-Two Diet and two potent cholesterol-lowering medications.2 Jayne faithfully followed her doctor’s orders for six months, although not without di culty. The medications nauseated her, and the diet kept her constantly hungry. Her condition was the talk of her friends and relatives, one of whom actually remarked to her, “I didn’t know a person could still be alive with a cholesterol of 750!” By the time Jayne returned for her recheck, she was desperate for improvement. And she had improved some, but not nearly enough. Her cholesterol had dropped from 750 mg/dl to 475 mg/dl and her triglycerides from 3,000 mg/dl to 2,000 mg/dl—an improvement to be sure, but still cause for great concern to both Jayne and her physician. They discussed

cause for great concern to both Jayne and her physician. They discussed her treatment options. Her doctor suggested either increasing the dosage of her cholesterol-lowering medications or adding yet another medicine to her regimen. Jayne wanted to think about it before she decided which option to take. She decided to do neither until she got a second opinion from another physician, so she came to our clinic. After listening to her history, we drew another blood sample and found that indeed she did have extraordinarily elevated levels of cholesterol and triglycerides in her blood—495 mg/dl and 1,900 mg/dl, respectively. In addition, her blood sugar was elevated to 155 mg/dl (normal is below 115 mg/dl), an ominous sign of impending diabetes. We instructed Jayne to stop taking both of her cholesterol-lowering medications and to change her diet drastically. Her new nutritional regimen allowed meat (even red meat), eggs, cheese, and many other foods that most people view as causing cholesterol problems, not solving them. We told her to call in three weeks to check in and to come back to have her blood checked in six weeks. She called at her appointed time and reported that she “felt grand” and that her nausea and hunger had vanished. The results of her blood work astounded her. Jayne’s cholesterol level had fallen to 186 mg/dl and her triglycerides to 86 mg/dl. Her blood sugar had dropped to 90 mg/dl; everything was back in the normal range. As you might imagine, she was ecstatic. How could this happen? How can a diet virtually everyone believes should raise cholesterol actually lower it—and in a person who doesn’t have just a slight cholesterol elevation but a major one? We know Jayne Bledsoe’s case is not a freak happenstance or an aberration because we’ve tried variations of the same regimen on countless other patients—all with the same results. The results make perfect sense, because Jayne’s problem, her illness, is not the elevated cholesterol level—that’s merely a sign of the underlying problem. Her problem is hyperinsulinemia, a chronic elevation of serum insulin. When Jayne rst came to our o ce, her insulin level was almost 20 mU/ml (milliUnits/milliliter), about double what we consider normal, which is anything below 10 mU/ml. After six weeks on a diet designed

which is anything below 10 mU/ml. After six weeks on a diet designed to lower her insulin level, Jayne’s lab work showed that she had dropped hers to 12 mU/ml, almost normal. By treating her real problem—excess insulin—we were able to solve her secondary problems of elevated cholesterol, triglycerides, and blood sugar. Standard medical therapies treat the symptoms of excess insulin— elevated cholesterol, triglycerides, blood sugar, blood pressure, and obesity—instead of treating the excess insulin itself. Unfortunately, the standard treatment of the symptoms may even raise the insulin levels and worsen the underlying problem. Excess Insulin: The Real Culprit A substance that fundamentally in uences every cell in the body, insulin is the master controller of the metabolic system without which all metabolic processes would be rudderless. Insulin is a hormone produced and secreted into the bloodstream by the pancreas, a glandular organ located behind the stomach, deep in the abdominal cavity. As it travels through the circulatory system insulin regulates the level of sugar in the blood—its most important function—and performs a thousand other tasks. Insulin, by activating or inhibiting various metabolic pathways, can make us sleepy, hungry, satis ed, dizzy, stuporous, or bloated. It can raise blood pressure, elevate cholesterol levels (as it did in Jayne Bledsoe’s case), cram fat into fat cells, cause the body to retain excess uid, damage arteries, and even change protein and sugar into fat. In the appropriate amount insulin keeps the metabolic system humming along smoothly with everything in balance; in great excess it becomes a rogue hormone ranging throughout the body, wreaking metabolic havoc and leaving a trail of chaos and disease in its wake. Although medical researchers have known of the bene cial e ects of insulin since the 1920s, when it was discovered, they have also generated an enormous amount of data over the past three decades showing that some of the effects are not so beneficial. Because there are no drugs available that can signi cantly reduce

Because there are no drugs available that can signi cantly reduce insulin levels, dietary manipulation is the only e ective treatment of insulin excess and the diseases it promotes (although exercise helps). That’s not to say that high blood pressure, for example, can’t be treated by medications; as everyone knows, it can be. But treating high blood pressure treats only the symptom and not the underlying cause. Hypertension and Heart Disease: The Insulin Connection Epidemiologists had long known that people with high blood pressure die from strokes and heart attacks at a much greater rate than those with normal blood pressure. By treating hypertension on a grand scale, medical scientists reasoned that they could signi cantly reduce the incidence of death caused by stroke and heart disease. Based on this reasoning and very little hard evidence, since no long-term hypertensive control studies had ever been done, the push was on to get Americans with high blood pressure diagnosed and medicated. At this point the rst long-term studies of the bene ts of treatment were just being started. Researchers at medical centers across the country were gathering groups of subjects with hypertension so that they could treat and carefully monitor them for the many years necessary for such studies to be valid. Statisticians performed their analytical alchemy and estimated that hypertension controlled with drugs decreased the incidence of deaths from heart disease and stroke—by 40 percent and 25 percent, respectively. How accurate were the statisticians? Not very, as it turns out. When the results were in, the researchers were astonished. The incidence of deaths due to stroke had fallen by approximately 25 percent—precisely what the statisticians had predicted; the gures for heart disease, however, weren’t even close. Rather than the predicted 40 percent decrease, the experts found no statistically signi cant decrease in deaths from heart disease compared to people who were not treated at all. People who ignored their hypertension and went on about their business didn’t develop heart disease at any greater rate than those who went to the expense and trouble of taking daily medications and assiduously monitoring their blood pressure. As you might imagine, this

discrepancy prompted a lot of head scratching among the scienti c establishment—especially in view of the fact that, based on their predictions, 19 million Americans were now spending upward of $4 billion annually on medicines to lower their blood pressure. What happened? How did the calculations go so far afield? As the researchers examined the data more closely, they found hypertension and heart disease are related through the common denominator of too much insulin—a discovery that spurred a tidal wave of new research. Since the excess insulin caused both the high blood pressure and the heart disease (through mechanisms we will explore in coming chapters), it becomes immediately obvious why reducing the blood pressure without reducing insulin levels would have little e ect on the progression of heart disease. A dismal postscript is that many of the medicines—diuretics and beta-blockers—actually increased insulin levels as they reduced blood pressure. So, ironically, many hypertensive patients taking medicine in the hope of preventing heart disease were encouraging the real culprit —excess insulin. In a great majority of these cases dietary control of elevated insulin levels could have eliminated both the high blood pressure and the threat of heart disease. Elevated insulin is Jayne Bledsoe’s problem. The diseases that insulin a ects directly—high blood pressure, elevated levels of cholesterol and other fats in the blood, diabetes, heart disease, and obesity—are the cause of the vast majority of death and disability in America today. They are the grim reapers of Western civilization. They kill more than twice the number of Americans each year than died in World War I, World War II, the Korean War, and Vietnam combined. How do we know that these disorders are actually caused by diet and not by some other factor or combination of factors? Just as with most aspects of medicine, some degree of uncertainty persists, but we’ve got a pretty good idea from data from three di erent research approaches —historical, current epidemiological, and direct experimental. And nothing in this book is theoretical—it’s all proven biochemistry found in any standard medical text—it’s simply never been put together in this way before.

The scienti c evidence will speak eloquently for itself, so let’s begin to examine these biochemical connections of diet and disease. The Bottom Line Virtually everyone is familiar with insulin as a regulator of blood sugar, and indeed that’s its main job in your body. But far beyond that, insulin can be called the master hormone of human metabolism, involved in the regulation of blood pressure, the production of cholesterol and triglycerides, and the storage of fat. When insulin levels become too high—a topic we’ll devote considerable discussion to throughout this book—metabolic havoc ensues with elevated blood pressure, elevated cholesterol and triglycerides, diabetes, and obesity all trailing along in its wake. These disorders are merely symptoms of a single more basic disturbance in metabolism—excess insulin and insulin resistance. There are no medications that treat excess insulin; a properly structured diet is the only means to bring it in line. (The usual low-fat, high-complex-carbohydrate approach won’t do it; it has just the opposite e ect.) Some medications—especially the betablockers and some diuretic medications, the very ones used to treat blood pressure and heart problems—actually make matters worse by causing the body to produce even more insulin, and doctor and patient get caught in the “symptom treatment trap.”

Here’s what usually happens: a patient gains weight and subsequently develops high blood pressure, for which the doctor prescribes a mild diuretic and low salt. The patient returns with better blood pressure but now a slight elevation in cholesterol and is put on a low-fat diet. He returns no lighter, with little change in cholesterol, but now his triglycerides or blood sugar have risen, too. The progression occurs because all these disorders are related through a single disturbance (excess insulin) that is actually being aggravated by the treatment. These disorders occur so commonly in our society that we’ve become numb to the staggering toll they take: heart disease, high blood pressure, and diabetes kill twice as many people every year as were killed in both world wars, Korea, and Vietnam combined. How do we know that these disorders are actually caused by diet and not by some other factor or combination of factors? Just as with most aspects of medicine, some degree of uncertainty persists, but we’ve got a pretty good idea from data from three di erent research approaches—historical, current epidemiological, and direct experimental. 1 Most of the case histories in this book are, like this one, actual patients whose names

have been changed. Occasionally a composite patient history is used to illustrate a particular point. 2 From the “Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults,” Archives of Internal Medicine 148:36-69, January 1988. Under these guidelines physicians treat

patients with elevated cholesterol in a stepwise fashion starting with dietary modi cation that limits fat to 30 percent and protein to 10 to 20 percent of calories and encourages the consumption of large amounts of carbohydrate. This is called the Step-One Diet. If the blood cholesterol level refuses to fall or doesn’t fall far enough on the Step-One Diet, a more stringent one that further reduces fat intake—the Step-Two Diet—follows. In those cases in which diet alone fails, most physicians turn to one or more of the many cholesterol-lowering drugs.

Chapter 3

Excess Insulin and the Insulin Resistance Syndrome One is unable to notice something—because it is always before one’s eyes. LUDWIG WITTGENSTEIN Philosophical Investigations

Consider how di erent life would be if we didn’t have the ability to store excess energy from the food we eat. Like the electric mixer that works only when it’s plugged in, we would have to be constantly hooked up to our energy source—food. At rst glance, this might not seem like such a bad idea. Many people nibble, snack, and munch their way through the day anyway, so wouldn’t it be grand if they could continue without the consequences of obesity, elevated cholesterol, and the other diseases of over-consumption? One obvious disadvantage would be that we would have to eat more food faster as we increased our intensity of activity. Let’s say we’re involved in a strenuous activity—swimming, for example. We could stu ourselves just before we jumped into the water, but that wouldn’t help. It would be like keeping the mixer plugged in for two hours before we used it, then unplugging it and turning it on. Nothing would happen because the mixer can’t store electricity. So we would have to eat while swimming. It would be cumbersome and inconvenient to have to gure out a way to consume food at all times—even during sleep. If we ate too much, it might be like plugging a mixer designed for 120 volts of electricity into a 240-volt circuit. What if we got stuck in an elevator and ate our way through all the food we had with us? As soon as the food was gone, we would sputter and choke out our last few moments like a car out of gas. Our survival would depend on always having adequate foodstu s immediately at hand, and any activity that had the potential to separate us from our food would be fraught with mortal danger. Our Built-In Battery

Did you know that, theoretically, most people could go for a couple of months without eating a single bite—some even up to a year or longer, depending on their degree of obesity? We can all eat ten meals a day or one or none; we can expend prodigious amounts of energy while eating little or no food, or we can eat prodigious amounts of food and expend almost no energy. In short, we have the capacity to use the energy from food we eat to meet our immediate needs and store the rest for later use. We have a built-in battery—the fat we carry on our bodies, which is replenished every time we eat and used for energy when we don’t. In fact the amount of fat on the body of an average person weighing 150 pounds contains enough energy to allow that person to walk from Miami to New York City without eating. Insulin and a few other hormones coordinate the activities of metabolism and ensure that our fat batteries work, making it possible for us to live unfettered by a constant power supply. Our metabolic systems precisely regulate the storage of excess food energy as fat and the release and breakdown of this body fat for the energy necessary for life. The metabolic system performs these tasks silently and without conscious effort on our part, but it is not foolproof. The Yin-Yang of Metabolism Insulin and glucagon are the primary hormones involved in the storage and release of energy within the body. When we eat, insulin drives our metabolism to store the excess food energy for use later. When later comes, glucagon drives the metabolism the other way, letting us burn our stored fat for the energy we need to swim or walk or sleep in the hours long after we’ve eaten. If we think of insulin as the hormone of feeding and storing and glucagon as the hormone of fasting and burning, it’s easy to see how people living in today’s America—with its abundance of food and never-stop-eating lifestyle—could be in the insulin-dominant mode most of the time. Although it performs countless other tasks throughout the body, insulin’s chief priority is to keep the blood sugar level from rising too

insulin’s chief priority is to keep the blood sugar level from rising too high. Glucagon’s main function is to prevent the blood sugar level from falling too low. The importance of this minute-by-minute regulation of the level of sugar in the blood is underscored by the fact that without either one of these hormones we would be dead in a matter of days or perhaps even hours. Without insulin the blood sugar would skyrocket, causing profound metabolic disturbances, dehydration, coma, and death. An absence of glucagon would allow the blood sugar to fall rapidly, bringing on brain dysfunction, somnolence, coma, and then death, because the brain requires blood sugar to operate properly. Because of this critical need to maintain the blood sugar in a narrow physiological band, the body doesn’t really much care about the secondary activities of these hormones as long as they keep the blood sugar where it’s supposed to be. And that’s what gets us in trouble. Can blood sugar regulate insulin and glucagon? Obviously it does. If blood sugar goes up, insulin goes up; conversely, if blood sugar falls, so does the insulin level, and the glucagon level rises. It’s this mechanism that gives us indirect control over our insulin and glucagon by manipulating our blood sugar level. No matter how hard we try, we can’t change our insulin and glucagon directly: we can’t use meditation or biofeedback, and we can’t take insulin or glucagon pills because these hormones are destroyed in the digestive process. Short of injecting ourselves with these hormones, the only way we can change our insulin and glucagon levels is to change our blood sugar level—which we can do in a hurry. If you want your insulin level to increase, just drink a sugary soft drink. Your blood sugar will climb, and so will your insulin level— within minutes. It’s a little more di cult, however, to increase glucagon levels. You’d somehow have to get your blood sugar level low enough to stimulate the pancreas to release glucagon. The only way to do this quickly is to give yourself an insulin injection. This extra insulin will drive the blood sugar low enough to stimulate the pancreas to release glucagon. Alternatively, you can wait around several hours without eating until your blood sugar falls enough on its own to bring about a surge of glucagon. Our blood sugar level governs the functioning of our entire metabolic

Our blood sugar level governs the functioning of our entire metabolic system. It’s at the top of the chain of command. When our blood sugar rises, it orders the metabolism to proceed along a certain course; when it falls, it gives the opposite orders. If our blood sugar, through the e orts of glucagon and insulin, controls our metabolism, and we can control our blood sugar level by eating or not eating certain foods, doesn’t it stand to reason that we can control our metabolism? Indeed we can. In fact this ability to control our metabolism is the foundation of our dietary program. INSULIN VS. GLUCAGON: TIPPING THE BALANCE Insulin—as part of its energy-storing behavior—activates a number of metabolic systems that we would just as soon not have activated, at least not on a perpetual basis. They were designed to operate on an intermittent, as-needed basis, but thanks to the aging process and the typical American diet, they tend to operate overtime. What systems are we talking about? The cholesterol synthesis system, for one. Insulin activates the enzymes that run the cholesterol-making apparatus, resulting in overproduction of cholesterol. Our own cells make cholesterol and lots of it. In fact, 70 to 80 percent of the cholesterol burbling along in your blood vessels was made by your own body. Only 20 to 30 percent came from your diet. Every cell in the body has the capacity to make cholesterol, but most is made in the liver, the intestines, and the skin, with the vast majority coming from the liver cells. Elevated levels of insulin spur these cells to churn out vast amounts of cholesterol, leading to elevated blood levels. You might wonder why nature designed it this way. Storing excess food energy as fat seems reasonable, but why make cholesterol? Excess food energy increases blood sugar, which increases insulin, which triggers the storage cycle leading to fat accumulation. To store fat and build muscle, the body must make new cells, and insulin acts as a growth hormone for this process. Cholesterol plays a vital role in this building and storing process; cholesterol provides the structural framework for all cells. In fact, if all of the cholesterol in your body

framework for all cells. In fact, if all of the cholesterol in your body were suddenly to vanish, you would dissolve into a puddle just like the Wicked Witch in The Wizard of Oz when Dorothy threw the water on her. Unfortunately, excess insulin stimulates excess cholesterol, and therein lies the problem. Excess insulin also encourages the proliferation and growth of smooth muscle cells in the linings of our arteries, an activity that causes a couple of problems. The larger muscle cells thicken the arterial walls, making them less elastic and reducing the volume inside the arteries. Less elastic, smaller coronary arteries are more prone to develop plaque and arterial spasm, the underlying causes of heart disease. Because the heart has to develop greater pressure to force the blood through the narrow, thickened arteries throughout the rest of the body, elevated blood pressure results. To compound this problem, insulin also causes the kidneys to retain salt and uid, which adds to the blood volume, increasing the pressure even more. Let’s not, however, neglect glucagon, its opposite. Be cause glucagon is the hormone of fat burning and fatty tissue breakdown, it reverses the building and storage processes set in motion by insulin. Under glucagon stimulation, the body gets rid of fat by burning it for energy. Since the body requires no extra cholesterol to help rid itself of cells, glucagon shuts down the production of cholesterol and helps send it on its way out of the circulation. The body doesn’t need extra uid to burn fat, so glucagon prompts the kidneys to get rid of it. Glucagon stimulates the breakdown and disappearance of the smooth muscle overgrowth in the arteries and lessens the incidence of arterial spasm. It’s easier to see the whole scenario for these two master hormones in chart form so that you can compare them more easily. THE ROLES OF INSULIN AND GLUCAGON INSULIN GLUCAGON lowers elevated blood sugar raises low blood sugar shifts metabolism into storage

shifts metabolism into storage shifts metabolism into burning mode mode converts glucose and protein converts protein and fat to glucose to fat converts dietary fat to storage converts dietary fats to ketones and sends them to the tissues for energy removes fat from blood and releases fat from fat cells into the blood transports it into fat cells for use by tissues as energy increases the body’s decreases the body’s production of production of cholesterol cholesterol makes the kidneys retain makes the kidneys release excess fluid excess fluid stimulates the growth of stimulates the regression of arterial arterial smooth muscle cells smooth muscle cells stimulates the use of glucose stimulates the use of fat for energy for energy Scanning this chart, it doesn’t take a rocket scientist to see that the more time we spend on the glucagon side, the better o we are. Remember, however, that metabolism control is not a one-or-the-other phenomenon: all insulin or all glucagon. Both hormones are present in the blood all the time. What drives the metabolism to store or to burn is a dominance of one or the other. How Food Affects Insulin and Glucagon Scientists have fed research subjects all kinds of food in all kinds of combinations, drawn their blood, and measured its insulin and glucagon to discover how foods a ect these hormones. The results of

glucagon to discover how foods a ect these hormones. The results of these experiments are in the following chart. INFLUENCE OF FOOD ON INSULIN AND GLUCAGON TYPE OF FOOD INSULIN GLUCAGON Carbohydrate +++++ no change Protein ++ ++ Fat no change no change Carbohydrate and Fat ++++ no change ++ Protein and Fat ++ High Protein and Low Carbo ++ + High Carbo and Low Protein ++++++++ + As you can see from the chart, of the three basic constituents of food —fat, protein, and carbohydrate—carbohydrate makes the most profound change in insulin, because it makes the most profound change in blood sugar level. Fat doesn’t do anything; as far as insulin is concerned, fat doesn’t exist. The combination of carbohydrate and protein, especially large amounts of carbohydrate with small amounts of protein, causes the greatest increase in insulin, a most enlightening fact, considering the typical American diet. What We Eat What does the typical American eat? How about the old standard: meat and potatoes—protein and carbohydrate. A hamburger and fries— protein and carbohydrate. A pizza, which is basically cheese, meat, and a crust—carbohydrate and protein. Macaroni and cheese—carbohydrate and protein. Think of anything we commonly eat: eggs and hash browns, milk and cereal, pork and beans, chicken and dumplings,

browns, milk and cereal, pork and beans, chicken and dumplings, peanut butter and jelly, ice cream, chili con carne, lasagne—the list could go on forever; every one of these popular foods is a combination of lots of carbohydrate and some protein. And lots of fat, of course, which we will consider shortly. Let’s forget about the protein for a minute and concentrate on just the carbohydrates that we eat, which do an outstanding job of raising insulin all by themselves. The second National Health and Nutrition Examination Survey (NHANES II) conducted by the National Center for Health Statistics published data in 1983 on the food consumption patterns of Americans.1 What would you guess as the number-one food consumed by the most Americans? White bread, rolls, and crackers— almost pure carbohydrate. How about number two? Doughnuts, cookies, and cake—more carbohydrate and fat. Number three, alcoholic beverages. All in all, of the top twenty foods Americans eat, eleven are virtually pure carbohydrate, four are a combination of carbohydrate and protein, and only ve are pure protein or a combination of protein and fat. These last five represent only 12 percent of the calories we eat. What about the fat and cholesterol we’ve shrugged o in our discussion so far? Do we not have to worry about them at all? Don’t they cause some problems? Sure they do, but not nearly the problems that carbohydrates do. And when dietary fat and cholesterol do cause problems, it’s usually because of the carbohydrate eaten along with them. It is true that fat is the raw material from which the body makes cholesterol, and it is also true that if you add more fat to your diet your cholesterol will increase, but only if you continue to eat a lot of carbohydrate at the same time that you add the fat. Although fat is the raw material the body uses to make cholesterol, insulin runs the cellular machinery that actually makes it. If you reduce the level of insulin, the cells can’t convert the fat to cholesterol, almost no matter how much fat is available. Eating fat in the absence of carbohydrate and expecting it to be converted to cholesterol is like trying to make your car go faster by putting a larger gas tank in it. If you reduce the amount of carbohydrate when you add the fat, not only will you probably not see any increase; you could even see a reduction in cholesterol levels. Sadly, the typical American diet is almost all fat and carbohydrate.

Sadly, the typical American diet is almost all fat and carbohydrate. According to the National Research Council’s Committee on Diet and Health in 1985, 46 percent of calories in the average American’s diet came from carbohydrate, 43 percent from fat, and a paltry 11 percent from protein: 89 percent of the American diet is fat and carbohydrate. THE SKINNY JUNK-FOOD JUNKIE AND OTHER PARADOXES Knowing how insulin works can help us analyze and make sense of seemingly contradictory data. The Harris poll completed in 1990 for Prevention magazine presents what appears on the surface to be inconsistent data. Americans scored 66.2 out of 100 in this survey on a variety of health-promoting practices, up from 61.5 percent in 1983, the rst year the survey was taken. What health-promoting practices? Eating less fat, eating less cholesterol, as we’d expect. The survey reported that although fewer Americans were making an e ort to avoid or restrict sugar, sweets, and other re ned carbohydrates, all in all our healthful behavior “has improved signi cantly since 1983, with greater numbers of individuals actively watching key elements of their diet such as their cholesterol level.” You would think that with this “signi cant” improvement in dietary behavior over the past seven years and the reported reduction of fat and cholesterol intake the population would have less high blood pressure and obesity, and fewer cholesterol problems. The survey didn’t look into the rst two, but it did address obesity. It reported that 64 percent of adult Americans, or about 100 million people, were overweight, up from 58 percent in 1983. If the nutritional establishment is right, and fat and cholesterol are the problems, with more people following such a “healthful” diet you would expect to see a reduction in obesity. The survey found just the opposite. You may nd speci c examples that seem to run contrary to the idea that elevated insulin causes the host of problems we’ve been discussing. We have a friend, for example, who has a son who might as well be connected by hose to a tank of sugar water. This kid always has a can of some kind of soft drink in his hand. He eats candy bars, cookies, cupcakes, and ice cream nonstop. His favorite foods are “spaghetti,

pizza, Cap’n Crunch cereal, and toast.” He eats at least 500 grams of carbohydrate per day, a gure that converts to over 2 cups of pure sugar. (Any carbohydrate is metabolized exactly like sugar.) But the kid is rail thin, and his cholesterol is only 135 mg/dl. What’s going on? Is he a statistical aberration, like the one relative in every family who smokes and drinks unremittingly, and lives to be ninetyfive? Although he does eat more sugar than many teenagers, this young man is not very di erent from most youngsters in America today They all eat way too much sugar and other re ned carbohydrates but seem to su er no ill e ects from it. Studies done both in the United States and in England indicate that many children from the ages of about ve up to adolescence consume approximately 200 grams, or about 1 cup, of sugar per day. That’s 1 cup of pure sugar, not total carbohydrate; total carbohydrate intake is much greater, about twice as much. So the data show that children eat excessive amounts of sugar and other carbohydrate, but anyone who looks can see that the vast majority of children are not fat. And if you checked their cholesterol levels and blood pressure—as we have done—you’d nd that almost all would be within the normal range or even low. Although today’s kids are twice as fat as they were a generation ago,2 you still see relatively few fat kids because most children don’t have an insulin problem—yet. But age and their diet and their genes nally catch up with them. After thirty or forty years of growing older on a high-carbohydrate diet, their intricately meshed metabolic gears start to slip, and they begin to develop obesity, high blood pressure, and all the rest. By then they will have an insulin problem. In childhood the insulin-blood sugar regulation mechanism works perfectly. When you’re a kid and you eat ice cream or drink a soda loaded with sugar, your blood sugar starts to rise and your pancreas releases a little insulin, which drives your blood sugar back down pronto. The pancreas releases just a small amount of insulin to force the blood sugar back down to normal because in childhood the cells are extremely sensitive to insulin. Small amounts of insulin translate into

low insulin levels. And due to this delicate sensitivity, small amounts of insulin easily handle even the outrageous amounts of sugar and other carbohydrates that kids stu themselves with—but not without a price. That price is a developing loss of sensitivity of the sensors to insulin—a condition known as insulin resistance—and chronically elevated insulin levels. Insulin Resistance: When Only Too Much Is Enough When cells become resistant to insulin, the receptors on their surfaces designed to respond to insulin have begun to malfunction. No clear cause for this malfunctioning has yet emerged from ongoing research, but the odds are it will be a combination of inherited tendency and lifestyle abuse. It simply means that the receptors require more insulin to make them work properly in removing sugar from the blood. Whereas before they needed just a touch to lower it, now they need a continuous supply of excess insulin to keep blood sugar within the normal range. As time goes by, blood sugar rises higher and stays up longer after the carbohydrate meal despite the enormous amount of insulin mustered to lower it. Bear in mind that were your doctor to check blood sugar during this stage of developing insulin resistance, your blood sugar would be perfectly normal. The major silent change taking place is the ever-growing quantity of insulin needed to keep it that way. Only by checking your blood insulin level—a lab test most doctors don’t even consider yet—can you determine whether you have an elevated insulin level (the condition called hyperinsulinemia) or insulin resistance. Hyperinsulinemia means simply having too much insulin in the blood, whereas insulin resistance means that the receptors no longer respond properly to insulin. This is the classic story of the chicken and the egg: which came rst? Researchers are not yet certain, but the preponderance of evidence points to excess insulin as the culprit. It’s not the little spurts of insulin that we see in children and adolescents after they eat carbohydrates that cause problems; these are

adolescents after they eat carbohydrates that cause problems; these are perfectly normal. It is the sustained elevated insulin levels— hyperinsulinemia—of the insulin-resistant adult that lead to the high blood pressure, cholesterol elevation, diabetes, and excess weight of midlife. Hyperinsulinemia is the real problem; all the other “problems” are merely the symptoms. If you look back at the chart showing the roles of insulin and glucagon, you can easily see what kinds of mischief hyperinsulinemia causes and how all these symptoms develop. Picture all the processes listed on the left side operating full blast—as they do under full insulin stimulation—and you can imagine the degree of harm being done silently. Unfortunately, most doctors treat only the symptoms and often in a way that makes the real problem worse. If you go on a low-fat diet, what happens? By decreasing your fat intake you usually decrease your protein intake, because virtually all foods that are protein-rich contain substantial amounts of fat. Meat, eggs, cheese, most dairy products—the best sources of complete dietary protein—are all either taboo or severely restricted on a low-fat diet. With this protein and fat restriction, the only food component left in the diet is carbohydrate, which by default results in your eating a high-carbohydrate, low-protein diet—the very diet that maximizes insulin production. If you had hyperinsulinemia to begin with—and if you have elevated triglycerides and cholesterol and high blood pressure, you can bet that you do— increasing your body’s production of insulin isn’t going to help. Instead of attacking the root cause of the problem, you’ll leave the doctor’s o ce with a prescription for a high blood pressure medicine, a more stringent diet, and perhaps a prescription for a cholesterol-lowering medicine as well. You are relieved, your doctor is happy, and the drug companies are ecstatic: they have just signed you on as a new customer to the tune of between $50 and $200 per month for life. If these methods bring about only cosmetic solutions to blood pressure, cholesterol, and other problems, how can we actually treat these disorders and make them go away? All you need to do is treat the hyperinsulinemia, and the other disorders improve or disappear. The only method available to treat hyperinsulinemia is diet.

Fortunately the dietary approach works spectacularly well. You can treat elevated cholesterol with the standard low-fat cholesterol-lowering diet with limited success until the cows come home, but you can reduce your insulin level with our program in a matter of days and see an almost immediate reduction of blood pressure, a signi cant reduction in your cholesterol or triglyceride levels in a few weeks, and a steady loss of excess stored body fat in the weeks and months ahead. It’s important to remember, however, that even though the regimen works rapidly to return insulin sensitivity to normal in most people, it works only as long as you follow it. It doesn’t return you to your childhood levels of imperviousness to carbohydrate assault. You must continue to follow the guidelines to maintain the changes; a return to your former eating habits will return you to your former problems. This nutritional structure is successful because it works with your metabolic system instead of counter to it; it’s been proven again and again around the world. Better in the Bush: Aborigines and Insulin Resistance The concept of undertaking nutritional therapy for disease by constructing a diet of reduced carbohydrate is beautifully illustrated in the work of Dr. Kerin O’Dea, an Australian physician, and her colleagues, who have extensively studied the Australian aborigines over the past decade or so. The aborigines are an interesting group in that they develop a high incidence of hyperinsulinemia and type II diabetes when exposed to an urbanized, Western diet. Like a huge number of Americans, they are genetically predisposed to the development of these disorders, but they develop them much more quickly. This situation, although unfortunate for the aborigines, makes them ideal candidates for the study of the relationship between diet and hyperinsulinemia. Dr. O’Dea began her studies by looking at the baseline insulin and glucose levels of urbanized aborigine subjects who were consuming a Western diet. She found that both the insulin and the glucose levels

were signi cantly elevated, which should come as no surprise when we consider the diet they were eating: “white our, white sugar, white rice, carbonated drinks, alcoholic beverages (beer, port), powdered milk and cheap fatty meat.” This sounds a lot like the diet of the majority of teenagers in America today. When we look at the composition of this diet in terms of the three nutrient types, we nd that it is “high in re ned carbohydrate (40-50%) and fat (40-50%) and relatively low in protein (< or = 10%)” or almost precisely the same composition as the typical American diet. Dr. O’Dea then started these people on her experimental diet, which she designed to approximate the original native diet they would consume were they back in the bush: considerable protein, not a lot of fat, and very little carbohydrate. The nutrient composition was “protein 70-75%, fat 20-25%, [and] carbohydrate